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We performed a laboratory analysis&#44; revealing mildly elevated chlorine &#40;114mEq&#47;l&#41;&#44; with normal renal function and all other ion parameters &#40;sodium&#58; 138mEq&#47;l&#59; potassium&#58; 4&#46;2mEq&#47;l&#41;&#44; and baseline arterial gasses compatible with a diagnosis of metabolic acidosis &#40;pH&#58; 7&#46;24&#59; pCO<span class="elsevierStyleInf">2</span>&#58; 33mm Hg&#59; pO<span class="elsevierStyleInf">2</span>&#58; 67mm Hg&#59; bicarbonate&#58; 17mmol&#47;l&#59; base excess &#91;BE&#93;&#58; -9&#46;1mmol&#47;l&#41;&#46; The anion GAP value &#40;difference between serum sodium and the sum of chlorine and bicarbonate&#41; was 7mEq&#47;l&#46; The patient received treatment with systemic steroids and quinolones&#44; with rapid clinical improvement until reaching a normal baseline levels&#46; However&#44; later controls revealed persistent hyperchloremic metabolic acidosis&#59; after ruling out other possibilities&#44; we attributed this fact to the chronic treatment with topiramate&#44; which was suspended and replaced with phenytoin&#44; which completely resolved the altered laboratory values by the time the patient was discharged&#46;</p><p class="elsevierStylePara">Topiramate is a sulphamate with anti-epileptic effects&#44; and is indicated in preventative treatment of migrane&#44;<span class="elsevierStyleSup">1&#44;2</span> the treatment of neuropathic pain<span class="elsevierStyleSup">3</span>&#44; bipolar disorder&#44;<span class="elsevierStyleSup">3</span> tobacco dependence&#44; and bulimia nervosa&#44;<span class="elsevierStyleSup">4</span> among other pathologies&#46; Its most common secondary side effects<span class="elsevierStyleSup">2&#44;5</span> are asthenia&#44; dizziness&#44; drowsiness&#44; emotional lability&#44; and weight loss&#46; The development of urolithiasis and hyperchloremic metabolic acidosis with a normal anion GAP is much less common&#44; but has been reported&#46; Topiramate has a molecular structure very similar to acetazolamide<span class="elsevierStyleSup">2&#44;6</span> and inhibits the carbonic anhydrase enzyme&#44;<span class="elsevierStyleSup">3&#44;6</span> especially the type II isoenzyme that predominates in human kidneys&#46;<span class="elsevierStyleSup">1&#44;2&#44;6</span> This can lead to mixed renal tubular acidosis<span class="elsevierStyleSup">1</span> &#40;type 3&#41; as a result of ultrafiltration and reabsorption of bicarbonate in both proximal and distal tubules&#44;<span class="elsevierStyleSup">4</span> thus altering urine acidification and provoking a decrease in serum bicarbonate and CO<span class="elsevierStyleInf">2</span> concentrations&#44;<span class="elsevierStyleSup">4</span> which is usually mild and asymptomatic&#44;<span class="elsevierStyleSup">7&#44;8</span> although can produce hyperventilation&#44;<span class="elsevierStyleSup">3&#44;4</span> neurological symptoms&#44;<span class="elsevierStyleSup">3</span> nephrolithiasis&#44; osteoporosis&#44; and osteomalacia in the long term&#46; The circumstances that predispose patients to developing this complication are not well established&#44; but patients are more likely to develop it if they have other conditions that cause acidosis&#44; such as infections&#44; diabetic ketoacidosis&#44; chronic renal failure&#44; or surgery&#46;<span class="elsevierStyleSup">4&#44;5</span> Certain genetic polymorphisms in the involved carbonic anhydrase isoenzymes may explain a greater or lesser susceptibility of certain patients to develop this complication&#46;<span class="elsevierStyleSup">3&#44;9</span> Some authors have suggested the possibility of monitoring bicarbonate<span class="elsevierStyleSup">1&#44;6</span> or CO<span class="elsevierStyleInf">2</span><span class="elsevierStyleSup">3&#44;5</span> levels to predict these cases&#44; although this is not a completely validated method&#46; The development of metabolic acidosis during chronic treatment with topiramate is a reversible condition&#44; regardless of the dosage<span class="elsevierStyleSup">3&#44;9</span> and duration of treatment&#46;9 The only treatment is to suspend the use of the drug10 &#40;there is no antidote&#41; and replace it with a substitute&#46; When the withdrawal of the drug is not possible&#44; and the patient maintains acceptable levels of pH and serum bicarbonate&#44; with no symptoms&#44; indefinite treatment with oral alkaline supplements can be administered &#40;sodium citrate or citric acid1&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">The authors affirm that they have no conflicts of interest related to the content of this article&#46;</p>"
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Topiramate-induced metabolic acidosis: a case study
Acidosis metabólica inducida por topiramato: a propósito de un caso.
Lucía Fernández-de Oruetaa, Javier Esteban-Fernándeza, Harald F.J. Aichnera, Ángel Casillas-Villamora, Sergio Rodríguez-Álvareza
a Servicio de Medicina Interna, Hospital Universitario de Getafe, Getafe, Madrid,
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    "textoCompleto" => "<p class="elsevierStylePara">We present the case of a 75 year-old male with hypertension and chronic obstructive pulmonary disease who was diagnosed with chronic delusional disorder and mixed personality disorder&#44; along with partial epilepsy due to a left parietal haematoma from several years prior&#46; The patient was under treatment with topiramate&#44; levetiracetam&#44; quetiapine&#44; sertraline&#44; clobazam&#44; and bronchodilators&#46; He sought treatment for a respiratory infection and functional deterioration consisting of apathy&#44; drowsiness&#44; and periods of aggressive behaviour&#46; A physical examination revealed that the patient had no fever&#44; although he did suffer from disorientation and slurred speech&#44; and would drift off to sleep&#44; but with no apparent focal loss of motor function&#46; The patient also had shallow tachypnoea&#44; widespread rhonchi&#44; and crackles in the left base&#44; with radiological images indicative of superinfection of the abnormally widened bronchial tubes&#46; We performed a laboratory analysis&#44; revealing mildly elevated chlorine &#40;114mEq&#47;l&#41;&#44; with normal renal function and all other ion parameters &#40;sodium&#58; 138mEq&#47;l&#59; potassium&#58; 4&#46;2mEq&#47;l&#41;&#44; and baseline arterial gasses compatible with a diagnosis of metabolic acidosis &#40;pH&#58; 7&#46;24&#59; pCO<span class="elsevierStyleInf">2</span>&#58; 33mm Hg&#59; pO<span class="elsevierStyleInf">2</span>&#58; 67mm Hg&#59; bicarbonate&#58; 17mmol&#47;l&#59; base excess &#91;BE&#93;&#58; -9&#46;1mmol&#47;l&#41;&#46; The anion GAP value &#40;difference between serum sodium and the sum of chlorine and bicarbonate&#41; was 7mEq&#47;l&#46; The patient received treatment with systemic steroids and quinolones&#44; with rapid clinical improvement until reaching a normal baseline levels&#46; However&#44; later controls revealed persistent hyperchloremic metabolic acidosis&#59; after ruling out other possibilities&#44; we attributed this fact to the chronic treatment with topiramate&#44; which was suspended and replaced with phenytoin&#44; which completely resolved the altered laboratory values by the time the patient was discharged&#46;</p><p class="elsevierStylePara">Topiramate is a sulphamate with anti-epileptic effects&#44; and is indicated in preventative treatment of migrane&#44;<span class="elsevierStyleSup">1&#44;2</span> the treatment of neuropathic pain<span class="elsevierStyleSup">3</span>&#44; bipolar disorder&#44;<span class="elsevierStyleSup">3</span> tobacco dependence&#44; and bulimia nervosa&#44;<span class="elsevierStyleSup">4</span> among other pathologies&#46; Its most common secondary side effects<span class="elsevierStyleSup">2&#44;5</span> are asthenia&#44; dizziness&#44; drowsiness&#44; emotional lability&#44; and weight loss&#46; The development of urolithiasis and hyperchloremic metabolic acidosis with a normal anion GAP is much less common&#44; but has been reported&#46; Topiramate has a molecular structure very similar to acetazolamide<span class="elsevierStyleSup">2&#44;6</span> and inhibits the carbonic anhydrase enzyme&#44;<span class="elsevierStyleSup">3&#44;6</span> especially the type II isoenzyme that predominates in human kidneys&#46;<span class="elsevierStyleSup">1&#44;2&#44;6</span> This can lead to mixed renal tubular acidosis<span class="elsevierStyleSup">1</span> &#40;type 3&#41; as a result of ultrafiltration and reabsorption of bicarbonate in both proximal and distal tubules&#44;<span class="elsevierStyleSup">4</span> thus altering urine acidification and provoking a decrease in serum bicarbonate and CO<span class="elsevierStyleInf">2</span> concentrations&#44;<span class="elsevierStyleSup">4</span> which is usually mild and asymptomatic&#44;<span class="elsevierStyleSup">7&#44;8</span> although can produce hyperventilation&#44;<span class="elsevierStyleSup">3&#44;4</span> neurological symptoms&#44;<span class="elsevierStyleSup">3</span> nephrolithiasis&#44; osteoporosis&#44; and osteomalacia in the long term&#46; The circumstances that predispose patients to developing this complication are not well established&#44; but patients are more likely to develop it if they have other conditions that cause acidosis&#44; such as infections&#44; diabetic ketoacidosis&#44; chronic renal failure&#44; or surgery&#46;<span class="elsevierStyleSup">4&#44;5</span> Certain genetic polymorphisms in the involved carbonic anhydrase isoenzymes may explain a greater or lesser susceptibility of certain patients to develop this complication&#46;<span class="elsevierStyleSup">3&#44;9</span> Some authors have suggested the possibility of monitoring bicarbonate<span class="elsevierStyleSup">1&#44;6</span> or CO<span class="elsevierStyleInf">2</span><span class="elsevierStyleSup">3&#44;5</span> levels to predict these cases&#44; although this is not a completely validated method&#46; The development of metabolic acidosis during chronic treatment with topiramate is a reversible condition&#44; regardless of the dosage<span class="elsevierStyleSup">3&#44;9</span> and duration of treatment&#46;9 The only treatment is to suspend the use of the drug10 &#40;there is no antidote&#41; and replace it with a substitute&#46; When the withdrawal of the drug is not possible&#44; and the patient maintains acceptable levels of pH and serum bicarbonate&#44; with no symptoms&#44; indefinite treatment with oral alkaline supplements can be administered &#40;sodium citrate or citric acid1&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">The authors affirm that they have no conflicts of interest related to the content of this article&#46;</p>"
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                  "referenciaCompleta" => "Burmeister JE, Pereira RR, Hartke EM, Kreuz M. Topiramate and severe metabolic acidosis: case report. Arq Neuropsiquiatr 2005;63:532-4. <a href="http://www.ncbi.nlm.nih.gov/pubmed/16059613" target="_blank">[Pubmed]</a>"
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                  "referenciaCompleta" => "García Gil D, Pérez V, Asencio C, García-Torrejón J. Acute topiramete toxicity to suicidal attempt. Med Clin (Barc) 2009;133:766-7."
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